PMID- 17389778
OWN - NLM
STAT- MEDLINE
DCOM- 20070813
LR  - 20181201
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 85
IP  - 3
DP  - 2007
TI  - Plasticity in the melanotrope neuroendocrine interface of Xenopus laevis.
PG  - 177-85
AB  - Melanotrope cells of the amphibian pituitary pars intermedia produce 
      alpha-melanophore-stimulating hormone (alpha-MSH), a peptide which causes skin 
      darkening during adaptation to a dark background. The secretory activity of the 
      melanotrope of the South African clawed toad Xenopus laevis is regulated by 
      multiple factors, both classical neurotransmitters and neuropeptides from the 
      brain. This review concerns the plasticity displayed in this intermediate lobe 
      neuroendocrine interface during physiological adaptation to the environment. The 
      plasticity includes dramatic morphological plasticity in both pre- and 
      post-synaptic elements of the interface. Inhibitory neurons in the 
      suprachiasmatic nucleus, designated suprachiasmatic melanotrope-inhibiting 
      neurons (SMINs), possess more and larger synapses on the melanotrope cells in 
      white than in black-background adapted animals; in the latter animals the 
      melanotropes are larger and produce more proopiomelanocortin (POMC), the 
      precursor of alpha-MSH. On a white background, pre-synaptic SMIN plasticity is 
      reflected by a higher expression of inhibitory neuropeptide Y (NPY) and is 
      closely associated with postsynaptic melanotrope plasticity, namely a higher 
      expression of the NPY Y1 receptor. Interestingly, melanotrope cells in such 
      animals also display higher expression of the receptors for thyrotropin-releasing 
      hormone (TRH) and urocortin 1, two neuropeptides that stimulate alpha-MSH 
      secretion. Possibly, in white-adapted animals melanotropes are sensitized to 
      neuropeptide stimulation so that, when the toad moves to a black background, they 
      can immediately initiate alpha-MSH secretion to achieve rapid adaptation to the 
      new background condition. The melanotrope cell also produces brain-derived 
      neurotrophic factor (BDNF), which is co-sequestered with alpha-MSH in secretory 
      granules within the cells. The neurotrophin seems to control melanotrope cell 
      plasticity in an autocrine way and we speculate that it may also control 
      presynaptic SMIN plasticity.
FAU - Jenks, Bruce G
AU  - Jenks BG
AD  - Department of Cellular Animal Physiology, Radboud University Nijmegen, Nijmegen, 
      The Netherlands. b.jenks@science.ru.nl
FAU - Kidane, Adhanet H
AU  - Kidane AH
FAU - Scheenen, Wim J J M
AU  - Scheenen WJ
FAU - Roubos, Eric W
AU  - Roubos EW
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20070327
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Adaptation, Physiological/*physiology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism/physiology
MH  - Calcium Signaling/physiology
MH  - Melanotrophs/metabolism/*physiology
MH  - Models, Biological
MH  - Models, Neurological
MH  - Neuronal Plasticity/*physiology
MH  - Neurosecretory Systems/*physiology
MH  - Pituitary Gland, Intermediate/physiology
MH  - Synapses/physiology
MH  - Xenopus laevis/*physiology
RF  - 72
EDAT- 2007/03/29 09:00
MHDA- 2007/08/19 09:00
CRDT- 2007/03/29 09:00
PHST- 2007/02/01 00:00 [received]
PHST- 2007/02/22 00:00 [accepted]
PHST- 2007/03/29 09:00 [pubmed]
PHST- 2007/08/19 09:00 [medline]
PHST- 2007/03/29 09:00 [entrez]
AID - 000101434 [pii]
AID - 10.1159/000101434 [doi]
PST - ppublish
SO  - Neuroendocrinology. 2007;85(3):177-85. doi: 10.1159/000101434. Epub 2007 Mar 27.